The close proximity of lymphoid components and fibroblasts in inflammatory sites implicates these lymphocytes and macrophages in the regulation of fibroblast function. Our current investigations deal with how the cellular interactions between the lymphoid system and fibroblasts may regulate connective tissue metabolism in both normal tissue repair and in pathological conditions associated with inflammatory reactions. Macrophages can be activated by a variety of agents including endotoxin, muramyl dipeptide or lymphokines to produce biologically active molecules (monokines). One of these monokines can cause fibroblasts to actively migrate or chemotax. Another monokine produce by activated macrophages stimulates fibroblasts to divide. These fibroblasts also become metabolically activated, generating enhanced levels of prostaglandins, collagen and proteins. In addition to the macrophages, inflammatory lesions may contain lymphocytes which when stimulated by specific antigens also influence fibroblast functions by the release of soluble mediators (lymphokines). Lymphocyte and macrophage products may thus provide a molecular and collagen deposition which accompany inflammation.